Stress Cardiomyopathy Due to Exogenous Thyrotoxicosis From T3 Supplementation

Abstract

Background: Wilson’s Temperature Syndrome (WTS) refers to a constellation of nonspecific symptoms, some of which include a low-normal body temperature, headaches, and fatigue. WTS was rejected by the American Thyroid Association as a valid medical diagnosis in 2005. Originally proposed in 1990 by Dr. E Denis Wilson, the etiology was theorized to be an impaired ability to convert T4 to T3, although this was not corroborated in thyroid lab abnormalities. Despite being publicly rebuffed as a true medical diagnosis, WTS has continued to gain traction amongst certain alternative medical groups and is treated with T3 supplementation. The development of a stress cardiomyopathy due to T3 supplementation is rare. Extrapolating from endogenous thyroid mediated stress cardiomyopathy and T4 supplementation induced stress cardiomyopathy, the pathophysiologic mechanism is likely excessive sympathetic activation. Clinical Case: A 58-year old female with no prior cardiac history presented to the emergency department with chest pain. Physical exam revealed a euvolemic appearing women, with intact and symmetric distal pulses, and a normal cardiac exam without murmurs or other abnormal heart sounds. There were no abnormal lung sounds. Her O2 sats were normal on room air. EKG and CXR were unremarkable. Her troponin was elevated (3.7 ng/mL, n< 0.034 ng/mL) and her BNP was elevated (4,568 pg/mL, n< 150 pg/mL). The patient was given aspirin and started on therapeutic heparin given concern for NSTEMI. Echocardiogram revealed an ejection fraction of 30% with hypokinesis of the entire apex and mid ventricle, raising concern for a stress cardiomyopathy.Coronary angiogram was performed which demonstrated no coronary artery disease. The patient underwent a cardiac MRI which confirmed a stress cardiomyopathy. Meanwhile, her laboratory workup was completed which revealed an undetectable TSH, a low T4 (0.53 ng/dL, n 0.7-1.8 ng/dL), and an elevated T3 (6.37 pg/mL, n 1.71-3.71 pg/mL). Patient endorsed taking oral liothyronine (T3) at doses of 5-40 mcg BID over the past 6 weeks per her alternative medicine provider for treatment of WTS. Her stress cardiomyopathy was presumed to be due to her exogenous thyrotoxicosis from T3 supplementation. She was counseled on the importance of cessation of T3 supplementation, and was started on heart failure medications. On hospital day 3, her T3 normalized to 2.73 pg/mL, and T4 remained low (0.4 pg/mL). Follow-up echocardiogram four months later demonstrated an ejection fraction that had improved to 45%. Conclusion: This case highlights the importance of physician awareness of alternative medicine diagnoses and treatment regimens that affect thyroid hormones and may cause harm to patients. This case is an important reminder of the effect thyroid hormones have on coronary vasculature, myocytes and myocardial function.